ArticleCells2022
In Vitro Characterization of Doxorubicin-Mediated Stress-Induced Premature Senescence in Human Chondrocytes.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- CD5L is a potential negative regulator of chondrocyte apoptosis in osteoarthritis.Osteoarthritis and cartilage open · 2026Article
- GW9508-Induced Activation of GPR40 in Thymic Epithelial Cells: A Therapeutic Strategy to Delay Thymic Aging.Aging cell · 2026Article
- Protocol to quantify cell-surface vimentin on senescent human chondrocytes and other cell types via a cell-based ELISA.STAR protocols · 2026Article
- Targeting breast cancer senescence in 3D models of bone metastasis.Breast cancer (Tokyo, Japan) · 2026Article
- Class I histone deacetylases and their inhibitors as targets to modulate cellular senescence in osteoarthritis.GeroScience · 2026Article
- Mitochondrial quantity-quality imbalance in cellular senescence: practical readouts and minimal assay bundles.BMB reports · 2026Review
- Comparative phenotypic and molecular profiling of replicative and chemically-induced senescence in articular chondrocytes.Cell death discovery · 2026Article
- Targeted Clearance of Senescent Endothelium by GPNMB-Specific CAR-T Cells.Journal of immunology research · 2026Article
- Targeting the CXCL12/CXCR4 pathway by an optimized derivative or EPI-X4 preserves chondrocyte function and offers a novel therapeutic approach in rheumatic diseases.Arthritis research & therapy · 2025Article
- Growth/Differentiation Factor 15 Promotes a Pro-Regenerative Response in Chondrocytes Upon Cartilage Injury.MedComm · 2025Article
- Single-cell sequencing reveals a senescent immune landscape in bone marrow lesions inducing articular cartilage damage in osteoarthritis.Bone research · 2025Article
- Multiomics Profiling of Extracellular Vesicles Supports Their Involvement in Endothelial Senescence-Associated Vascular Dysfunction.Journal of extracellular biology · 2025Article
- Doxorubicin Induces a Senescent Phenotype in Murine and Human Astrocytes.Journal of neurochemistry · 2025Article
- Generation of an In Vitro Cartilage Aging Model Using Human Sera from Old Donors.Bioengineering (Basel, Switzerland) · 2025Article
- Development of Reliable and High-Throughput Human Biomimetic Cartilage and Bone Models to Explore Senescence and Personalized Osteoarthritis Treatment Options.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025Article
- Article
- MiR-668-5p targets ZNRF3, an E3 ubiquitin ligase to enhance osteoblast function and alleviate senescence in doxorubicin-induced age-related bone loss.Frontiers in endocrinology · 2025Article
- Article
- Cellular senescence impairs tendon extracellular matrix remodeling in response to mechanical unloading.Aging cell · 2024Article
- Endoplasmic reticulum stress-induced senescence in human lung fibroblasts.American journal of physiology. Lung cellular and molecular physiology · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulation of senescent chondrocytes is thought to drive inflammatory processes and subsequent cartilage degeneration in age-related as well as posttraumatic osteoarthritis (OA). However, the underlying mechanisms of senescence and consequences on cartilage homeostasis are not completely understood so far. Therefore, suitable in vitro models are needed to study chondrocyte senescence. In this study, we established and evaluated a doxorubicin (Doxo)-based model of stress-induced premature senescence (SIPS) in human articular chondrocytes (hAC). Cellular senescence was determined by the investigation of various senescence associated (SA) hallmarks including β-galactosidase activity, expression of p16, p21, and SA secretory phenotype (SASP) markers (IL-6, IL-8, MMP-13), the presence of urokinase-type plasminogen activator receptor (uPAR), and cell cycle arrest. After seven days, Doxo-treated hAC displayed a SIPS-like phenotype, characterized by excessive secretion of SASP factors, enhanced uPAR-positivity, decreased proliferation rate, and increased β-galactosidase activity. This phenotype was proven to be stable seven days after the removal of Doxo. Moreover, Doxo-treated hAC exhibited increased granularity and flattened or fibroblast-like morphology. Further analysis implies that Doxo-mediated SIPS was driven by oxidative stress as demonstrated by increased ROS levels and NO release. Overall, we provide novel insights into chondrocyte senescence and present a suitable in vitro model for further studies.
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